ReviewCells2021
Aberrant Splicing Events and Epigenetics in Viral Oncogenomics: Current Therapeutic Strategies.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- DMS-informed secondary structure modeling of Epstein-Barr Virus LMP-1 pre-mRNA defines novel elements spanning introns.PloS one · 2026Article
- From viruses to cancer: exploring the role of the hepatitis C virus NS3 protein in carcinogenesis.Infectious agents and cancer · 2024Review
- Review
- The immunogenetics of COVID-19.Immunogenetics · 2023Review
- Splicing Characterization and Isoform Switch Events in Human Keratinocytes Carrying Oncogenes from High-Risk HPV-16 and Low-Risk HPV-84.International journal of molecular sciences · 2023Article
- Microbiomes, Epigenomics, Immune Response, and Splicing Signatures Interplay: Potential Use of Combination of Regulatory Pathways as Targets for Malignant Mesothelioma.International journal of molecular sciences · 2022Review
- Viral Encoded miRNAs in Tumorigenesis: Theranostic Opportunities in Precision Oncology.Microorganisms · 2022Review
- Epstein-Barr Virus Enhances Cancer-Specific Aberrant Splicing of TSG101 Pre-mRNA.International journal of molecular sciences · 2022Article
- ViMIC: a database of human disease-related virus mutations, integration sites and cis-effects.Nucleic acids research · 2022Article
- The endogenous HBZ interactome in ATL leukemic cells reveals an unprecedented complexity of host interacting partners involved in RNA splicing.Frontiers in immunology · 2022Article
- Alternative RNA splicing in cancer: what about adult T-cell leukemia?Frontiers in immunology · 2022Review
- The Catastrophic HPV/HIV Dual Viral Oncogenomics in Concert with Dysregulated Alternative Splicing in Cervical Cancer.International journal of molecular sciences · 2021Review
- Characterization of a Novel Viral Interleukin 8 (vIL-8) Splice Variant Encoded by Marek's Disease Virus.Microorganisms · 2021Article
- Viral Manipulation of the Host Epigenome as a Driver of Virus-Induced Oncogenesis.Microorganisms · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Global cancer incidence and mortality are on the rise. Although cancer is fundamentally a non-communicable disease, a large number of cancers are known to have a viral aetiology. A high burden of infectious agents (Human immunodeficiency virus (HIV), human papillomavirus (HPV), hepatitis B virus (HBV)) in certain Sub-Saharan African countries drives the rates of certain cancers. About one-third of all cancers in Africa are attributed to infection. Seven viruses have been identified with carcinogenic characteristics, namely the HPV, HBV, Hepatitis C virus (HCV), Epstein-Barr virus (EBV), Human T cell leukaemia virus 1 (HTLV-1), Kaposi's Sarcoma Herpesvirus (KSHV), and HIV-1. The cellular splicing machinery is compromised upon infection, and the virus generates splicing variants that promote cell proliferation, suppress signalling pathways, inhibition of tumour suppressors, alter gene expression through epigenetic modification, and mechanisms to evade an immune response, promoting carcinogenesis. A number of these splice variants are specific to virally-induced cancers. Elucidating mechanisms underlying how the virus utilises these splice variants to maintain its latent and lytic phase will provide insights into novel targets for drug discovery. This review will focus on the splicing genomics, epigenetic modifications induced by and current therapeutic strategies against HPV, HBV, HCV, EBV, HTLV-1, KSHV and HIV-1.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.